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Pharm II > Lecture 2 (Cardio)-Exam1 > Flashcards

Lecture 2 (Cardio)-Exam1 Flashcards

1
Q

What does Aldosterone do normal and when blocked?

A
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2
Q

What is steps one, two, and three of primary homeostasis?

A

(1) Vasoconstriction – endothelin
* Reflexive contraction of vessel
* Decreased blood flow (dec. bleeding)

(2) Exposure – exposed collagen from damaged endothelium releases vWF
* vWF binds to the exposed collagen

(3) Adhersion-platelets bind to vWF via glycoprotein 1B (GP1B)
* After vWF is bound to collagen

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3
Q

What is step 4 of primary hemostasis?

A

Activation – active platelets change shape (release chemicals)
* Release more vWF, serotonin, ADP, and thromboxane A2, Ca (important for clotting)
* ADP and thromboxane A2
* Activate more platelets
* Stimulate expression of glycoprotein IIB/IIIA on platelet membrane surface

ADP = adenosine diphosphate

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4
Q

What is step five of primary hemostasis?

A

Aggregation – GPIIB/IIIA links platelets together via fibrinogen and form a platelet plug

Platelet plug to move to secondary hemostasis

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5
Q

Fill in for antiplatelet drugs

A
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6
Q

Antiplatelet therapy: Aspirin
* What is the MOA of aspirin?
* What type of drug is it?

A
  • Activated platelets release arachidonic acid
  • AA is onverted to prostaglandins via COX1 -> prostaglandins releases thromboxane A2
  • Thromboxane A2 promotes activation of more platelets and activation of glycoprotein 2b/3a
  • Aspirin is an irreversible COX inhibitor
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7
Q

Antiplatelet therapy: Aspirin
* Blocks what for and for how long?
* First line for what?

A
  • Blocks thromboxane platelet activation for the life of the platelet (7-10 days)
  • First-line prophylactic antiplatelet therapy
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8
Q

Antiplatelet therapy: ADP receptor inhibitors (P2Y12 inhibitors)
* What are the examples?
* Second line for what?
* What can it be combined with?

A
  • Clopidogrel, ticagrelor, ticlopidine, prasugrel
  • Second-line prophylactic antiplatelet therapy
  • Combined with aspirin for dual antiplatelet therapy (DAPT)
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9
Q

What is the MOA of ADP receptor inhibitors (P2Y12 inhibitors)?

A
  • Bind to the P2Y12 ADP receptor and prevent ADP from binding
  • No ADP binding = no formation of glycoprotein 2b/3a receptors on the surfaced of activated platelets
  • No platelet aggregation
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10
Q

Antiplatelet therapy: Glycoproteint 2b/3a inhibitors
* What are the examples?
* Higest risk of what?
* Only available how?
* Use has what?
* How long do you use it?
* Always given with what?

A
  • Abciximab, eptifibatide, tirofiban
  • Highest risk of bleeding and thrombocytopenia
  • Only available IV
  • Use has declined with the use of DAPT
  • < 24-hour duration
  • Always given with heparin
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11
Q

Antiplatelet therapy: Glycoproteint 2b/3a inhibitors
* What is the MOA?
* What is the medication reserved for?

A

MOA:
* Prevent platelet cross linking and aggregation

Reserved for use with interventional cardiac procedures in high-risk patients
* NSTEMI with high cTn
* STEMI not preloaded with a P2Y12 inhibitor

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12
Q

Antiplatelet Therapy:
* What are the indications?
* What are the CI?

A
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13
Q

Bleeding with antiplatelet agents:
* What are the sxs of bleeding (low or dysfunctional platelets)?

A
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14
Q

Bleeding with antiplatelet:
* Serious bleeding rare – MC when?
* CI when?

A
  • Serious bleeding rare – MC when combined with other anticoagulants
  • CI: any active bleeding
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15
Q

Antiplatelet: Aspirin
* What is the MOA?
* What are the SE?
* CI if what?

A
  • Irreversible COX-1 inhibitor
  • SE: GI bleeding and Dyspepsia
  • CI only if true allergy
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16
Q

Clopidogrel
* What is the MOA?
* What are the SE?

A

MOA:
* Irreversible P2Y12 receptor blocker
* Prodrug – requires activation in liver by CYP450 enzymes; mostly CYP2C19

SE:
* Dizziness
* Headache
* Palpitations
* GI distress
* Thrombocytopenia

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17
Q

Clopidogrel
* Avoid use with what?
* Poor efficacy with what?

A
  • Avoid use with CYP2C19 inhibitors – decrease concentration of active metabolites (decreased efficacy)
  • Poor efficacy with low CYP2C19 metabolizers
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18
Q

Prasugrel
* What is the MOA?
* What are the SE?
* Similar to what?

A
  • Irreversible P2Y12 receptor blocker-> Prodrug – requires activation in liver by CYP2C19
  • SE: Same as Clopidogrel (Dizziness, Headache, Palpitations, GI distress, Thrombocytopenia)
  • Equal efficacy to clopidogrel with more bleeding risk
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19
Q

Ticagrelor
* What is the MOA?
* What are the SE?

A

MOA:
* Reversible P2Y12 receptor blocker
* Not a prodrug
* Metabolized by CYP3A4

SE:
* Dyspnea
* Nausea
* Dizziness
* Hyperuricemia

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20
Q

Cangrelor:
* What is the MOA?
* Only what?

A
  • Reversible P2Y12 receptor blocker
  • Only IV P2Y12 inhibitor
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21
Q

Wha tis stable angina? What unstable angina?

A
  • Stable Angina: Myocardial ischemia secondary to exertion (imbalance between myocardial oxygen demand and delivery)
  • Unstable Angina: New, worsening symptoms with activity and/or at rest
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22
Q

What is NSTEMI and STEMI?

A
  • NSTEMI/NSTE-ACS: Myocardial infarction without ST elevation
  • STEMI/STE-ACS: Myocardial infarction with ST elevation
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23
Q

Stable Angina:
* MC with what?
* What is the most common cause?
* When does pain happen?
* how is the pain?
* Symptoms include what?

A
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24
Q

Stable angina:
* What is the one txt approach of risk factor modification?

A
  • Slow progression of atherosclerosis and prevent complications
  • Minimum effect on symptom control or QOL
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25
Q

For stable angina risk factor modification txt, fill in (focus on Lipid and BP management)

A
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26
Q

For stable angina risk factor modification txt, fill in

A
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27
Q

Ace inhibitors/ARBS
* Decreases what?
* Who is this recommended to?

A
  • Decrease the incidence of cardiovascular death and time to myocardial infarction or stroke in patients with ASCVD
  • Class I recommendation by the AHA / ACC for all patients with SIHD and HTN, DM, CKD, HFrEF
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28
Q

Ace inhibitors/ARBS
* What are all the benefits?

A
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29
Q

What is the first line antiplatelet therapy for stable angina ?
* What does it block?
* What is the dose? Why?
* Decreases what?

A
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30
Q

What is the second line antiplatelet therapy for stable angina ?

A

Second-line: clopidogrel
* Aspirin intolerant or contraindicated

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31
Q

Stable angina/ stable ischemic heart disease
* How do you manage angina?

A

Decrease ischemic episodes and increase the amount of exercise / exertion prior to chest pain
* Minimal survival benefit
* Improves symptoms and QOL

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32
Q

Management of stable angina-Acute sx with NITRATES
* What is the MOA?
* What predominates? What does that cause?
* Decreases what?
* What does it increase?
* What else does it dilate and what is the cause?

A
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33
Q

Nitroglycerin
* What is the Route?
* What is the onset?
* What are the indication?
* What are the SE?

A

*Headaches usually resolve in 2 to 3 weeks with chronic use and are generally responsive to acetaminophen
**Concomitant beta blocker administration may preven

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34
Q

What is CI with Nitrates?

A

CI: Right-sided infarct – hypotension and concomitant use with drugs for ED

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35
Q

Acute symptomact treatment: (stable ang)
* What is first line?
* What can the first line be used for?
* What is the Primary effect and secondary effects?

A
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36
Q

Nitroglycerin:
* What is the MC route?
* What is the dose?

A
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37
Q

Nitroglycerin-patient education
* What do you need to say about storage? (3)
* Refill when if open?
* What does the patient do before taking it?
* Keep it where when you take it?
* Take when?
* Call 911 when?

A
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38
Q

Management of stable angina-prevention:
* What is first line?
* What is the MOA?
* All of them are what?
* What is not as effective?
* Not indicated for what disease?

A
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39
Q

Management of stable angina-prevention:
* What is second line? Why would a patient take this?
* Decrease what?
* What is the MOA?
* What are the examples?

A
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40
Q
A
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41
Q

Fill this in for the prevention of stable angina

A

Considered 3rd line-long acting nitrates
* Need a nitro free period therefore your body does not get use to it

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42
Q

Nitroglycerin tolerance:
* Can occur when?
* What does it impair?
* How do you prevent it? How do you do that? What is the issue?

A
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42
Q

Stable angina-revascularization:
* PCI or CABG may be indicated in some patients with stable angina. What happened with sxs, mortality and symtom control?

A
  • Persistent symptoms despite maximum medication and lifestyle changes
  • Does not improve mortality in this population
  • May provide symptom control

AL-Lamee et al Lancet 2018
* 200 patients randomized to PCI or sham procedure
* No difference in angina episode frequency, QOL scores or exercise treadmill time between groups

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43
Q

Vasospastic angina
* What is it?
* Less what?
* What is it caused why?
* What type of ischemia?
* Patients generally are what?
* What is it assoicated with?

A
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44
Q

Vasospatic angina
* What is the treatment?

A
  • Acute attacks – SL nitroglycerin
  • Chronic suppression – calcium channel blockers
  • Avoid beta-blockers
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45
Q

Acute coronary syndromes (ACS) encompasses what?

A

ACS encompasses Unstable angina, NSTEMI, and STEMI
* NSTE-ACS: NSTEMI and Unstable Angina
* STE-ACS: STEMI

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46
Q

acute coronary syndrome:
* What are changed that suggest change from stable angina to ACS?

A
  • Sudden onset of new angina
  • Angina at rest
  • Increased severity of stable angina (> 20 minutes)
  • Atypical symptoms – SOB, fatigue, dizziness
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47
Q

What do you need to order and give with the clinical suspicion of ACS?

A
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48
Q

Sorry, I know it is a lot for one card but it was more simple things lol

Initial assessment-All ACS Patients
* Assess what?
* What do you need get a preliminary of?
* What dx test?
* What nees to be attached to patient?
* Give what in needed?
* What needs to be obtained?
* What needs to be brought to bedside?
* Rule out what?

A
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49
Q

Initial supportive care: all ACS
* What do you need to give? (4)

A
  • Aspirin given – 325 mg chew and swallow x 1 dose
  • Nitroglycerin given – 0.4 mg up to 3 doses if no contraindications
  • Morphine – reserved for severe chest pain not relieved by nitroglycerin – not routine (only if cont. CP)
    * Retrospective studies showed increased risk of death
    * Mechanism unknown
  • Beta-blocker within first 24 hours
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50
Q

What are the contraindications of nitroglycerin?

A
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51
Q

Unstable
* What is it caused by?
* What happens to vessle?
* What are the ECGs changes?
* What is the risk straify (2)

A
  • Ruptured atherosclerotic plaque
  • Usually ≥ 90% vessel occlusion
  • ± ECG changes: ST depression or T wave inversions
  • Risk stratify (TIMI, GRACE, HEART scores)
    * Low-risk – ischemia driven approach
    * Intermediate to high risk – early invasive approach

SAME AS NSTEMI

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52
Q

NSTEMI
* What is it caused by?
* What happens to vessle?
* What are the ECGs changes?
* What is the risk straify (2)

A
  • Ruptured atherosclerotic plaque
  • Usually ≥ 90% vessel occlusion
  • ± ECG changes: ST depression or T wave inversions
  • Risk stratify (TIMI, GRACE, HEART scores)
    * Low-risk – ischemia driven approach
    * Intermediate to high risk – early invasive approach

SAME AS UNSTABLE ANGINA

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53
Q

What makes Unstable angina and NSTEMI different?

A
  • Unstable: negative troponin (ischemia only)
  • NSTEMI: Positiv troponin (infarction)
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54
Q

NSTEMI: Low risk patients
* What is the management? (general)

A

Medical management – PCI not planned

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55
Q

NSTEMI: Low risk patients
* What type of therapy early?
* What are some other medications does the patient need to be on?

A
  • Early anticoagulation and antithrombotic therapy
  • Start P2Y12 inhibitor – clopidogrel or ticagrelor (they got aspirin already)
  • Initiate anticoagulation – enoxaparin or unfractionated heparin (doses vary)
    * Short-term, discontinued within a few days (unlike DVT)
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56
Q

NSTEMI: Low risk patients
* What happens if stress test positive?
* The medical management option is also preferred for who?

A
  • Non-invasive stress test – if positive proceed to angiography ± PCI, CABG
  • Also preferred for patients with serious comorbidities or contraindications to PCI
57
Q

NSTE-ACS: Intermediate to high-risk patients
* What type of patient usually has PCI within 24 hours?

A

Superior for patients
* > 70 years
* Previous MI or revascularization
* ST-segment changes
* Heart failure
* Elevated troponin
* Diabetes mellitus
* Positive non-invasive stress test

58
Q

Who else it is recommended for to have PCI within 24 hours?

A
  • Refractory angina
  • Acute heart failure
  • Cardiogenic shock
  • Arrythmias
59
Q

NSTE-ACSIntermediate to high-risk patients
* What is initiated?
* What is preferred for patients with early PCI? Why?
* What are the CI?

A
  • Prasugrel or ticagrelor preferred for patients with early PCI
  • Reduction in cardiovascular death, MI, or stroke compared to clopidogrel
  • Prasugrel with increased bleeding risk compared to ticagrelor
    * CI: stroke or TIA
60
Q

NSTE-ACS: Intermediate to high-risk patients
* Prasugrel and ticagrelor not recommended for use with what?
* Many patients de-escalated to what prior or shortly after hospital discharge? Why?

A
  • Prasugrel and ticagrelor not recommended for use with fibrinolytic therapy (aka – tPA)
  • Many patients de-escalated to clopidogrel prior to or shortly after hospital discharge due to changes in bleeding risk or cost
61
Q

NSTE-ACS: Intermediate to high-risk patients
* What do you need to initate besides P2Y12 inhibitor
* What needs to happen with 24 hours?

A
  • Initiate anticoagulation – enoxaparin or unfractionated heparin
  • Coronary angiography within 24 hours
62
Q

Initial txt of stemi
* What is first?
* What do you need to immediately do? What is the time goals? (2)

A
  • Initial supportive care=MONA
  • Immediate reperfusion – angiography / PCI
    * Goal reperfusion time = ≤90 minutes from arrival in PCI- capable hospital
    * 120 minutes if emergent transfer required
63
Q

Inital txt of STEMI
* What do you need to start after MONA?
* When do you give fibroinolysis?

A
  • Initiate P2Y12 inhibitor - any with PCI or clopidogrel with fibrinolysis
  • Initiate anticoagulation - heparin, LMWH, or bivalirudin
  • Fibrinolysis: Only when expected time to PCI is > 120 minutes
64
Q

What are the examples of fibrinolytics?
* What is the source?
* What is the MOA?

A
65
Q

What are the indications of TPA?

A
66
Q

What are the absolute contraindications of TPA?

A
67
Q

What are the absolute contraindications of TPA?

A
68
Q

Said FYI but no trust here lol

Fibrinolytics:

A
69
Q

Revascularization: Coronary bypass graft
* Useful in those with what?
* More efficacious in who?
* More beneficial in who?

A
  • Useful in those with left main coronary disease or 3 vessel disease (over 70% stenosis) and LV dysfunction
  • More efficacious in patients with diabetes
  • More beneficial in patients with low EF
70
Q

Revascularization: PCI
* What med is needed after? How long?

A

Stent placement standard – needs uninterrupted DAPT for minimum of 1 year

71
Q

Secondary prevention of ischemic event

A
72
Q

Secondary prevention of ischemic event

A
73
Q

Secondary prevention of ischemic event

A
74
Q

summary

A
75
Q

Cocaine related ACS
* Give what?
* Do NOT give what?

A
  • Give benzodiazepines as needed for symptom control
  • Do NOT give beta blockers
76
Q

ACS

  • What do you need to stop for all ACS patients?
  • Correct any what?
A
  • ­Stop NSAID therapy if possible
  • ­Correct any electrolyte abnormalities, especially hypokalemia and hypomagnesemia, which often occur together.
77
Q

Heart Failure:
* Inability of what?
* What does the body have to do?
* These mechanisms eventually do what?

A
  • Inability of the heart to provide sufficient output to meet metabolic demands of the body
  • The body has compensatory mechanisms in place to improve CO (makes everything worse)
  • These mechanisms eventually exacerbate the underlying cardiac problem
78
Q

Heart failure:
* Poor cardiac output= _ BP= _ tissue perfusion
* What dectects the BP and what does it stimulate?

A
  • Poor cardiac output = decreased BP = decreased tissue perfusion
  • Baroreceptors in the carotid and aortic sinuses detect low BP and stimulate the sympathetic nervous system ( NE and Epi to stimulate beta receptors -> mroe beta 1)
79
Q

Heart failure:
* After NE/Epi is released from sympathetic nervous system, what is stimulated?

A

Beta and alpha receptors

80
Q

Heart failure:
* What happens with beta receptor stimulation?

A
  • Bind to beta-1 cardiac receptors and increase HR and contractility
  • Bind to beta-1 receptors in kidneys and stimulate JG cells to release renin – RAAS cascade initated (increase BP becasue body is thinking you need more fluid which is not true)
81
Q

Heart failure:
* What happens with alpha receptor stimulation?

A
  • Bind to alpha receptors causing vasoconstriction
  • Increase total peripheral resistance
    * Venous constriction – increases venous return, preload, stroke volume, CO
    * Vasoconstriction of afferent arterioles of kidney decreases renal blood flow and stimulate kidneys to retain fluid
82
Q

Heart failure:
* What is the new result?

A
  • Heart rate increases – not enough time for bad heart to fill properly
  • Fluid retention – kidneys (various mechanisms)
  • Arterial constriction increases afterload
  • Venous constriction increases preload

Heart struggles

83
Q

Heart failure
* most txt is aimed to do what?

A

Most treatments aim to shut down compensatory mechanisms

84
Q

Heart Failure: HFrEF (systolic HF)
* What type of problem?
* What diseases?
* Reduced what?
* Rhythm?
* EF?

A
85
Q

HFpEF (diastolic HF)
* What type of problem?
* Not enough what?
* What are the causes?
* What is the EF?

A
86
Q

What are the sxs of left vs right sided HF?

A

Left-Pulmonary
Right- systemic

87
Q
A
88
Q
A
89
Q

HF-treatment goals? (4)?

A
  • Slow and reverse LV remodeling
  • Reduce symptoms
  • Improve quality of life
  • Reduce morbidity and mortality
90
Q

HF txt:
* Which drug classes are symtom relief only?

A

Diuretics, nitrates, digoxin symptom relief only

91
Q

HF: Which drugs deal with long-term management and to improve survival (decrease mortality)?

A
  • ACEI / ARBs
  • Beta blockers
  • Aldosterone antagonists
  • Angiotensin receptor/neprilysin inhibitors
  • Sodium-glucose co-transporter 2 inhibitors
92
Q

Pharm general prinicipals:
* Medications can be started how? What is usually started first then two weeks after?
* How do you start the classes of medications?

A
93
Q

What are the titration intervals for ACE/ARBS? ARNI/BB?hydralazine+nitrates?

A
  • ACE/ARBS – double dose every 1-2 weeks
  • ARNI/beta blockers/hydralazine + nitrates – double every 2 to 4 weeks
94
Q

What is Stage A and B of HF?

A
95
Q

What is stage C and D of HF?

A
96
Q

Stage A- Primary Prevention
* What needs to change in life?
* Stop what?
* What needs to get under control?

A
  • Lifestyle modifications: Physical activity, healthy diet, weight management
  • Smoking cessation
  • Hypertension – guideline directed BP control
97
Q

Stage A: Primary prevention
* What do you start with a patient with Type 2 DM and CVD or high ASCVD? What does it prevent?
* What else to you give for CDV?

A
98
Q

Stage B: Prevent symtomatic HF
* What do you need to start with LVEF <40%?
* What do you start with patients with recent MI or ACS?

A
99
Q

What do you need to avoid in a patient with LVEF <50%? Why? (2)

A
  • Thiazolidinedione hypoglycemics (rosiglitazone, pioglitazone)
  • Non-dihydropyridine CCB – negative inotropic effects
100
Q
A
101
Q

Stage C-Symptomatic HF: supportive measures
* What type of txt?
* Follow what?
* What do you need to address?

A
  • Multidisciplinary treatment
  • Follow guideline directed medical therapy (GDMT)
  • Address barriers to self care
    * Reduce hospitalizations
    * Improve survival
102
Q

Stage C-Symptomatic HF: supportive measures
* What do you need to give against resp illness?
* Screen for what?
* What about diet?
* What about movement?

A
  • Vaccination against respiratory illnesses
  • Screen for depression, social isolation, frailty, low health literacy
  • Sodium restriction (<2300 g/day); low level evidence
  • Exercise / cardiac rehabilitation - supervised
103
Q

STAGE C – HFrEF ARNI, ACEI, ARBS: NYHA class II to IV HF
* Reduce what?
* Lower rates?
* Lower incidence of what?

A
  • Reduce total mortality
  • Lower hospitalization rates
  • Lower incidence of MI or stroke
104
Q

Stage C– Hfref ARNI, ACEI, ARBs
* NYHA class II to III - What is recommended first line? Why?
* What is second and third line?

A
105
Q
  • What are Natriuretic peptides and their effects?
A

Natriuretic peptides – endogenous vasoactive peptides that reverse effects of angiotensin II (ATII)
* Promote fluid loss, vasodilation
* Decreased blood pressure
* Decreased cardiac hypertrophy

106
Q

Neprilysin inhibitors:
* What does Neprilysin usually do?
* what happens if blocked?
* What must the drug be given with?

A

Natriuretic peptides and ATII naturally broken down by neprilysin
* Neprilysin inhibition prevents the breakdown of natriuretic peptides
* Neprilysin inhibition prevents the breakdown of ATII

Must be given with ARB to counteract the effects of increased ATII

107
Q

Sacubitral/Valsartan (entresto)
* What are the adverse effects?
* What are the CI?

A
108
Q

Sacubitral/Valsartan (entresto)
* What do you need to monitor?
* What does the drug increases?

A
109
Q

Sacubitril / valsartan (entresto):PARADIGM HF trial
* What were the primary outcomes?

A

Primary outcomes – cardiovascular death and
hospitalizations rates

  • 21% of patients taking Entresto vs 26.5% of patient taking enalapril met primary outcomes (p<0.001)
  • Study stopped earlyðrules of benefit met
110
Q

Stage C-HFrEF BB
* Reduces, improves what?
* What are the specific agents shown to reduce mortality and hospitalizations?

A
111
Q

Stage C – HFrEF Beta-blockers
* What is the goal?

A

Goal = reach dose showing benefit in clinical trials
* Benefits seen across all patient populations
* Benefits are not a class effect

112
Q

Stage C-HFrEF MRAs
* What are the examples?
* What classes and what does it reduce?

A
113
Q

Stage C-HFrEF MRAs
* What should the patients have? (2)
* What do you need monitor closely?

A
114
Q

Stage C HFrEF SGLT2i
* Recommended to who?
* Independent of what?

A
  • SGLT2i recommended to reduce HF hospitalization and cardiovascular mortality in patients with or without type 2 DM (SYMPTOMS)
  • Independent of glucose lowering effects
115
Q

Stage C HFrEF SGLT2i
* What do the two trails look at? What are the results (3)

A

Two trials DAPA-F (dapagliflozin) and EMPEROR-REDUCED (empagliflozin)
* Patients had a LVEF ≤ 40 %, stage II-IV NYHA HF, and elevated natriuretic peptides

Results:
* 25% composite reduction in cardiovascular death or hospitalization
* Reduction in all cause mortality
* Slower decline in eGFR

116
Q
A
116
Q

Sodium-glucose co-transport 2 inhibitors

A
117
Q

Sodium-glucose co-transport 2 inhibitors
* Effectiveness decreases with what?
* Specific agents shown to decrease what?

A
  • Effectiveness decreases with reduction in renal function
  • Specific agents shown to decrease atherosclerotic CV morbidity and mortality
118
Q

Diuretics:
* What does it do?
* What is first line? Adjust dose to what? Reponse decrease by what?

A

Relief of fluid retention to improve symptoms

Loop diuretics = first line
* Adjust dose to euvolemia; weight loss 0.5 to 1 kg/day
* Response decreased by high sodium intake, NSAID use and renal impairment

119
Q

Diuretics: Thiazide Diuretics
* Recommended as what?
* Patients not responding to what?
* Decreases what?
* Dual therapy does what?

A
120
Q

Stage C: HFrEF (hydralazine and nitrates)
* Reduces what?

A

Relief of fluid retention to improve symptoms

121
Q

Stage C- HFrEF: Hydralazine and nitrates
* Who is it recommended for?
* What does it improve?

A
122
Q

She siad FYI

Aditional therapies
* What does it not do?
* May decrease what?
* What are the examples (4)

A
123
Q

Hfref – drugs without benefit / potential harm
* Which drug has no benefit?

A

Dihydropyridine CCBs

124
Q

Hfref – drugs without benefit / potential harm
* Which drugs cuase harm and why?

A
  • Nondihydropyridine CCB
  • IC antiarrhythmics and dronedarone – increased mortality
  • Thiazolidinediones – worsen symptoms and increase hospitalizations
  • DPP-4 inhibitors (gliptins) – increase HF hospitalizations
  • NSAIDS (increase sodium and BP)
125
Q

HFpEF (LVEF >50%)
* Therapy similar to what?
* What do you need to identify and treat?

A

Therapy similar to HFrEF – mostly symptomatic benefit
Identify and treat underlying causes
* Hypertension
* Amyloidosis / sarcoidosis
* CAD
* Atrial fibrillation

126
Q

HFpEF (LVEF >50%)
* Diuretic?
* What agents decrease hospitalization?
* What offer no benefit?

A

Diuretic therapy as per HFrEF (LOOP)

Agents decreasing hospitalization
* SGLT2i
* Mineralocorticoid receptor antagonists
* ARB or ARNI

Nitrates offer no benefit

127
Q

What are the four cardiomyopathies?

A
128
Q

Dilated CMP
* What are the causes?

A

(most common – 95%)
* Idiopathic / ETOH (first line-stop alc)
* Systolic dysfunction
* Low EF
* MC in men

129
Q

What are the causes of hypertrophic and restrictive cardiomyopathy?

A

Hypertrophic Cardiomyopathy
* Genetic
* Diastolic dysfunction

Restrictive Cardiomyopathy
* Idiopathic
* Systolic & diastolic dysfunction

130
Q

Dilated CMP txt
* What do you need to stop?
* Treat underlaying what?
* MCC of what?

A
  • Stop offending agent – drugs, ETOH, chemotherapy regimens
  • Treat underlying CAD / ischemia
  • MCC of heart transplantation
131
Q

Dilated CMP txt
* What guidelines do you need to follow?
* Why anticoagulations?
* Low LVEF < 35% and/or arrythmias may need what?

A

Follow guidelines for HFrEF
* Diuretics / sodium restriction / digoxin – symptom control
* ACEI, ARB, beta blockers, mineralocorticoid receptor antagonists – decrease mortality
* Do ARNi if meet criteria in HF

Anticoagulation for known atrial fibrillation, artificial valve, thrombus

Low LVEF < 35% and/or arrythmias may need assist devices / defibrillators

132
Q

Hypertrophic CM
* What is the organization of heart?
* What are the causes?
* Often what?

A
133
Q

Hypertrophic CM Txt
* Avoid what?
* Screen who?

A
  • Avoid strenuous exercise or competitive sports
  • Screen family members
134
Q

Hypertrophic CM
* How do you avoid preload reduction (increase preload)?
* How do you avoid afterload reduction (increase afterload)?

A

Avoid preload reduction – increases EDV and decreases outflow obstruction
* Adequate hydration
* Avoid diuretics
* Avoid venodilators – ACEI/ARBs/nitrates

Avoid afterload reduction – increases EDV and decreases outflow obstruction
* Avoid ACEI/ARBs/hydralazine/dihydropyridine CCB

135
Q

Hypertrophic CM txt
* Avoid increasing what?
* What is first line?
* What is second line?
* What do patients need to AVOID?

A
136
Q

Hypertrophic CM txt:
* How do you avoid fatal arrythmias?
* Why anticoags?
* What are some invasice procedures options?

A
137
Q

Restrictive cmp:
* What happens to heart?
* What are the primary and secondary causes?

A
138
Q

Restrictive CMP txt
* Treat what?
* What is the main stay txt?
* What nnes to be restricted?
* What is not generally beneficial
* What as needed (3)
* What type of transplat?
* What is poor?

A

Pharm II (14 decks)

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